Why host-directed therapies could transform bacterial infection treatment

Q. Congratulations on your Young Investigator Award and on being recognized as a touchINFECTIOUS DISEASES Future Leader. What does this recognition mean to you at this stage of your career?

Thank you. I think as an individual researcher, or as part of a research group, it is relatively straightforward to focus on doing science that is technically rigorous and robust, and to have confidence in that work internally.

What is often harder to achieve is broader reach and wider impact. So having the opportunity to speak about my research during the Young Investigator Awards session yesterday, and again through this interview, is something I really value. It is an excellent opportunity to share the work more widely, and I am very grateful for it.

Q. Your work spans infectious diseases, microbiology, and host immune responses to bacterial infections. What key experiences have shaped your research journey so far?

I’ve always found it curious that conventional antibiotics hold such a monopoly over the treatment of infection. I’ll use a fellow Scot, Alexander Fleming, as an example. Before discovering penicillin, his main focus was actually on host defense factors. He discovered lysozyme, one of the humoral innate immune factors, and was interested in the therapeutic application of substances like that before penicillin emerged.

I think there are several limitations to conventional antibiotics. Resistance is the most obvious, but there are others as well. They can cause microbiome toxicity, and they often do not adequately target intracellular bacterial populations, which are increasingly recognized as important in disease pathogenesis.

Other medical disciplines, particularly oncology, have shown that simply giving toxic agents to the problem—whether cancer cells or microbes, is not always the best strategy. Oncology has led the way with immunotherapies that have significantly improved outcomes. So overall, I’m interested in how we can augment immune responses as an alternative or adjunct to conventional antibiotics.

Q. As an emerging leader in the field, what opportunities or challenges do you think will define the future of infectious diseases research over the next few years?

I think aging and multimorbidity will be major themes. In health, the immune system does an extraordinary job protecting us from pathogens. If we take Staphylococcus aureus as an example, colonization is vastly more common than invasive disease, more than a thousand times more common, so clearly the immune system succeeds most of the time.

When people think about immune failure or immunodeficiency, they often think about rare genetic conditions or medical immunosuppression. But aging and common comorbidities also impair immune responses.

Given demographic changes around the world, I think susceptibility to infection driven by aging and multimorbidity will become increasingly important. That means we need to better understand which parts of the immune system fail in these settings, and how we can therapeutically recalibrate them using host-directed therapies.

Q. Based on your presentation, how could host-directed therapies and patient stratification improve outcomes in common bacterial diseases?

I think patient stratification is the first step. Most bacterial diseases are highly heterogeneous, but our ability to divide patients into mechanism-based subgroups, or endotypes, is still limited. Often, we do not fully understand why two patients infected with the same pathogen can have very different clinical outcomes.

A practical starting point is to classify patients into clinical subphenotypes based on observable features. That is some of the work I have done in Staphylococcus aureus bacteremia. The next step is to define the mechanistic differences between those patient groups. Once we understand that, it opens the door to targeted host-directed therapies.

For example, which patients with Staphylococcus aureus bacteremia have defective macrophage responses, and how might we correct that? If we continue to treat diseases such as Staphylococcus aureus bacteremia as a single entity, we risk dismissing treatments that may be beneficial for specific subgroups of patients.

Q. What are the next steps in your own research?

I’m very interested in the impact of age on host defense. Much of my work so far on macrophage host defense has used primary human macrophages taken from young, healthy donors, or mouse models using animals of a normal age that broadly reflect younger healthy humans. What I would really like to focus on next is how aging affects microbicidal responses, using clinical samples from older versus younger adults, and from people living with important comorbidities.

Q. What have been your highlights from ESCMID 2026, and what are you looking forward to next?

As someone very interested in Staphylococcus aureus disease, I’m particularly looking forward to Professor Asha Bowen speaking about the clindamycin results from the SNAP trial, a large international platform trial in Staphylococcus aureus bacteremia.

From a clinical microbiology perspective, I also really enjoyed the antibiogram interpretation session, especially discussions around emerging resistance mechanisms, new antimicrobials, and how to apply those findings in real-world practice.